Results of the experiments conducted during the first two years of funding leave little doubt that aging in mice is accompanied by profound decrease in the ability to resist infection with intracellular pathogens. The diminished ability to resist these infections appears to be mainly due to an impaired capacity of old mice to generate effective antibacterial specific immune mechanisms. The goals for the forthcoming year are to analyze, using experimental murine listeriosis as a model, the mechanistic basis for this age-determined loss in immune competence. Experiments will be conducted to seek answers as to whether there are age-dependent quantitative differences in the production of protective T-cells and whether old mice have a greater propensity for generating specific and nonspecific suppressor T-cells. It will also be determined whether the efficiency of "old" protective T-cells is lower because of a decreased ability to produce lymphokines. Studies on the effect of aging on the mobilization and activation of monouclear phagocytes during the course of an infection will also be initiated.